Histochemistry and Cell Biology最新文献

{"title":"Correction: Vitamin D receptor suppresses pulmonary fibroblast activation by downregulating the TGF-β1/Smad signaling pathway.","authors":"Jialai Yang, Tangbing Xu, Rui Xu","doi":"10.1007/s00418-026-02473-x","DOIUrl":"https://doi.org/10.1007/s00418-026-02473-x","url":null,"abstract":"","PeriodicalId":13107,"journal":{"name":"Histochemistry and Cell Biology","volume":"164 1","pages":""},"PeriodicalIF":2.1,"publicationDate":"2026-04-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147627604","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Fibre morphology, intramyocellular lipid content and 3D capillary architecture in human postural, respiratory and locomotor muscles in type 2 diabetes mellitus.","authors":"Nataša Pollak, Jiří Janáček, František Saudek, Erika Cvetko, Barbora Radochová, Armin Alibegović, Chiedozie Kenneth Ugwoke, Davide Alessandro Basello, Žiga Šink, Luka Pušnik, Rok Tit Tomazin, Nejc Umek","doi":"10.1007/s00418-026-02477-7","DOIUrl":"10.1007/s00418-026-02477-7","url":null,"abstract":"<p><p>In type 2 diabetes mellitus (T2DM), skeletal muscle is a major site of metabolic and microvascular dysfunction, yet most human data derive from large locomotor muscles, whereas postural and respiratory muscles remain less well characterised. We examined whether T2DM alters fibre morphology, intramyocellular lipid (IMCL) content, and three-dimensional (3D) capillary architecture across functionally distinct muscles. Postural (splenius capitis [SC]), respiratory (diaphragm [DIA]; external intercostal [EXT]), and locomotor (vastus lateralis [VL]) muscles from adult male individuals (T2DM versus control, n = 24/group) were sampled < 24 h post-mortem. Analysis included myosin heavy chain fibre typing, Sudan Black B intramyocellular lipid (IMCL) quantification, and 3D capillary morphometry (length, tortuosity, anisotropy, branching density). Groups were age-matched (T2DM 70.8 ± 7.4 versus 69.7 ± 11.8 years; p = 0.684), but body mass index (BMI) was higher in T2DM (31.9 ± 4.7 versus 24.8 ± 2.7 kg m^-2; p < 0.0001). Fibre-type profiles were similar, except for elevated 2a/2x hybrids in T2DM VL (p = 0.014). Mean fibre diameters were preserved, though type 1 fibres were larger in T2DM SC (p = 0.0238). IMCL was higher in T2DM SC and EXT (p < 0.05), with non-significant differences in VL and DIA. Type 1 and 2a fibres had higher IMCL than glycolytic fibres, with no group-by-fibre-type interaction. BMI strongly predicted VL IMCL (p < 0.0001), while age was negatively associated with IMCL in respiratory muscles (p ≤ 0.05). Capillary length per fibre volume was selectively reduced in DIA (p = 0.0115); other indices were preserved, except for higher anisotropy in EXT (p = 0.0495). Overall, these functionally diverse muscles showed subtle muscle-specific remodelling in T2DM, with adiposity-linked IMCL accumulation and reduced DIA capillary supply, although findings should be interpreted in the context of the post-mortem study.</p>","PeriodicalId":13107,"journal":{"name":"Histochemistry and Cell Biology","volume":"164 1","pages":""},"PeriodicalIF":2.1,"publicationDate":"2026-04-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13053442/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147622786","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Targeting SAT1 alleviates high glucose-induced tubular ferroptosis and fibrosis: implications for diabetic kidney disease.","authors":"Yingqi Tang, Siyao Wang, Yu Wang, Tianyuan Zhang, Yu Liu, Yunhua Di","doi":"10.1007/s00418-026-02464-y","DOIUrl":"https://doi.org/10.1007/s00418-026-02464-y","url":null,"abstract":"<p><p>Renal tubular damage and interstitial fibrosis are highly linked to diabetic kidney disease (DKD) progression. Ferroptosis in renal tubular epithelial cells has emerged as one of the key mechanisms of DKD. Spermidine/spermine N1-acetyltransferase 1 (SAT1) knockdown has been found to alleviate repetitive low-dose cisplatin-induced kidney damage and fibrosis, and importantly, SAT1 silencing represses cellular sensitivity to ferroptosis. However, the effect of SAT1 on DKD-associated ferroptosis and its potential mechanism remain understood. In this study, we constructed a high-fat diet/streptozotocin-induced DKD mouse model and a high glucose (HG)-injured HK-2 cell model with the aim of verifying whether SAT1 silencing attenuates DKD tubular damage by regulating ferroptosis. We found that SAT1 was upregulated in DKD mouse kidneys and HG-treated HK-2 cells. Significant tubular damage, fibrosis, ferroptosis, and oxidative stress were observed in DKD mouse kidneys. In an in vitro loss-of-function assay, SAT1 silencing suppressed HG-induced HK-2 cytotoxicity, extracellular matrix (ECM) synthesis, and inflammation. Additionally, SAT1 silencing decreased HG-activated MDA and 4-HNE production, while restoring GSH levels. SAT1 silencing also abrogated HG-activated ferroptosis in HK-2 cells, as evidenced by a reduction in iron overload, inhibition of lipid peroxidation, and upregulation of ferroptosis-related protein (SLC7A11, GPX4, and TFR1) expression. Mechanistically, SAT1 silencing facilitated nuclear translocation and expression of NRF2. Impairment of NRF2 function abrogated the inhibitory effects of SAT1 silencing on HG-stimulated HK-2 cytotoxicity, ferroptosis, and ECM accumulation. Overall, the SAT1/NRF2 axis is a critical regulator of tubular damage in DKD, and suppression of SAT1 may be an underlying target for DKD treatment.</p>","PeriodicalId":13107,"journal":{"name":"Histochemistry and Cell Biology","volume":"164 1","pages":""},"PeriodicalIF":2.1,"publicationDate":"2026-04-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147622806","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Histochemical characterization of muscularis macrophage loss and disruption of a miR-93-5p-AHNAK neuro-immune axis in Hirschsprung's disease.","authors":"Xiao Li, Lingyun Bu, Xiaoqing Wang, Long Li, Guoqiang Du, Rongde Wu, Wei Liu","doi":"10.1007/s00418-026-02466-w","DOIUrl":"https://doi.org/10.1007/s00418-026-02466-w","url":null,"abstract":"<p><p>Hirschsprung's disease (HSCR) is a congenital disorder of the distal intestine characterized by aganglionosis of the enteric nervous system. While defective migration of neural crest-derived precursors is a well-established hallmark, how the intestinal microenvironment contributes to impaired neuronal support remains poorly understood. Here, we combined histochemical analyses of human HSCR colon with functional assays to investigate the role of muscularis macrophages (MMs) and a miR-93-5p-AHNAK pathway in regulating enteric neurons. Using immunohistochemistry and immunofluorescence on ganglionic and aganglionic segments, we mapped the density, spatial distribution, and phenotype of MMs, and quantified the expression of miR-93-5p and its predicted target AHNAK. In vitro, polarized M2-like macrophages were cocultured with enteric neuronal cell lines to assess neuronal migration, proliferation, and apoptosis. Gain-of-function and loss-of-function approaches for miR-93-5p, together with a dual-luciferase reporter assay, were used to validate AHNAK as a direct target. M2-like MMs (CD163⁺/CD206⁺) were abundant around myenteric ganglia in ganglionic colon but reduced in aganglionic segments, where AHNAK expression was increased. M2 macrophages enhanced neuronal migration and proliferation and protected against apoptosis, whereas disruption of the miR-93-5p-AHNAK axis impaired these neuro-supportive effects. Together, our data identify a muscularis macrophage-miR-93-5p-AHNAK axis that supports enteric neurons and demonstrates that loss of M2-like MMs and dysregulated miR-93-5p-AHNAK signaling compromise neuronal homeostasis in HSCR. These findings add a histochemical microenvironment perspective to HSCR pathogenesis and support a candidate neuroimmune pathway for restoring immune-neuronal balance, pending in vivo and clinical validation.</p>","PeriodicalId":13107,"journal":{"name":"Histochemistry and Cell Biology","volume":"164 1","pages":""},"PeriodicalIF":2.1,"publicationDate":"2026-04-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147615947","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Time-dependent integrated tissue and circulating biomarker dynamics of spexin and progranulin in an experimental myocardial infarction model.","authors":"Sercan Kaya, Tuba Yalçin","doi":"10.1007/s00418-026-02471-z","DOIUrl":"10.1007/s00418-026-02471-z","url":null,"abstract":"<p><p>Inflammation, oxidative stress and apoptosis, in particular, play critical roles in the pathophysiology of myocardial infarction (MI). Isoproterenol (ISO) is a frequently used agent in experimental models to induce MI. This study aimed to determine the temporal changes in Spexin (SPX) and Progranulin (PRG) levels in an ISO-induced experimental MI model. The study consisted of control and ISO-treated groups (ISO-1, ISO-2, ISO-4, ISO-6 and ISO-24). In the ISO-induced MI model, serum CK-MB and troponin (I-T) levels increased, confirming cardiac damage. However, increases in oxidative parameters and decreases in antioxidant enzyme levels indicated cardiac oxidative stress. Furthermore, the time-dependent increase in inflammatory cell infiltration on histopathological examinations, paralleled by the increase in proinflammatory cytokines, confirmed the cardiac inflammatory response. Despite a decrease in cardiac antiapoptotic markers, the increase in proapoptotic marker levels reflected the temporal change in the apoptotic process induced by ISO administration. ISO administration caused SPX levels in serum and cardiac tissue to increase at 4 h and decrease at 24 h. The dynamic fluctuations in SPX levels may be related to adaptation to the stress responses and cardiac energy metabolism. ISO administration increased PRG levels in serum and cardiac tissue at 6 and 24 h. This increase suggests that PRG may contribute to a role particularly in inflammation and cardiac remodeling processes. In conclusion, the cardiac oxidative stress, inflammation and apoptosis induced by ISO administration further validated the experimental MI model. Changes in SPX and PRG levels in the ISO-induced MI model demonstrate their promise as cardiac potential markers.</p>","PeriodicalId":13107,"journal":{"name":"Histochemistry and Cell Biology","volume":"164 1","pages":""},"PeriodicalIF":2.1,"publicationDate":"2026-03-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13033465/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147573694","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"February in focus in HCB: spatial transcriptomics.","authors":"Douglas J Taatjes, Jürgen Roth","doi":"10.1007/s00418-026-02467-9","DOIUrl":"https://doi.org/10.1007/s00418-026-02467-9","url":null,"abstract":"","PeriodicalId":13107,"journal":{"name":"Histochemistry and Cell Biology","volume":"164 1","pages":""},"PeriodicalIF":2.1,"publicationDate":"2026-03-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147573724","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Electric field-induced inflammatory and angiogenic responses in rat female reproductive tissues: evidence for early extracellular matrix remodeling.","authors":"Ozlem Ozmen, Halil Asci, Oznur Kolay, Elif Nur Selcuk, Duygu Yuksel, Selcuk Comlekci, Pinar Karabacak","doi":"10.1007/s00418-026-02470-0","DOIUrl":"10.1007/s00418-026-02470-0","url":null,"abstract":"<p><p>High-intensity electric fields (EFs) are increasingly encountered in occupational and environmental settings, raising concerns regarding their potential biological effects on hormonally responsive organs. However, the cellular and molecular responses of female reproductive tissues to short-term exposure to high-voltage EFs remain insufficiently characterized. This study aims to investigate EF-associated histopathological and immunohistochemical alterations in major female reproductive organs. Forty adult female Wistar albino rats were randomly assigned to five experimental groups (n = 8 per group): a control group (0 min) and four EF-exposed groups subjected to a nominal electric field intensity of 10 kV/m EF for 1, 5, 15, or 30 min using a custom-designed parallel-plate exposure system. The field intensity was verified at predefined measurement points within the exposure setup. Ovaries, uterus, and uterine tubes were examined using hematoxylin-eosin staining and semi-quantitative histopathological scoring. Immunohistochemical analyses were performed to evaluate the expression of tumor necrosis factor-α (TNF-α), vascular endothelial growth factor (VEGF), and osteonectin as markers of inflammation, angiogenesis, and extracellular matrix remodeling. Exposure to the electric field was associated with time-dependent histopathological alterations, including tissue edema, hemorrhage, epithelial degeneration, and leukocyte infiltration. The most pronounced ovarian and uterine changes were observed in the 30-min exposure group, whereas the uterine tubes exhibited comparatively milder structural alterations. Immunohistochemical analysis demonstrated increased TNF-α and VEGF expression in higher-exposure groups, suggesting activation of inflammatory and angiogenic pathways. Osteonectin expression was elevated in all examined reproductive tissues and was also detected in regions without overt morphological damage, indicating its potential sensitivity to early tissue stress responses associated with EF exposure. Significant correlations were observed between histopathological injury scores and immunohistochemical marker expression levels. Overall, short-term exposure to high-intensity electric field was associated with inflammatory signaling, angiogenic responses, and extracellular matrix remodeling in female reproductive tissues in this experimental model. These findings provide histological and immunohistochemical evidence of tissue responses to EF exposure and underscore the need for further studies incorporating comprehensive exposure characterization and additional molecular endpoints to better define potential reproductive health implications to high-voltage electric fields.</p>","PeriodicalId":13107,"journal":{"name":"Histochemistry and Cell Biology","volume":"164 1","pages":""},"PeriodicalIF":2.1,"publicationDate":"2026-03-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13031200/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147528566","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Relationships between clusters of interchromatin granules and chromatin fibers.","authors":"Nicolas Thelen, Marc Thiry","doi":"10.1007/s00418-026-02465-x","DOIUrl":"https://doi.org/10.1007/s00418-026-02465-x","url":null,"abstract":"<p><p>Among nuclear compartments, interchromatin granule clusters (IGCs) are widely regarded as biomolecular condensates implicated in the regulation of gene expression, leading to the production of distinct mRNA species. Nevertheless, their functional dynamics within the nuclear environment remain largely elusive. In this study, we employed multiple transmission electron microscopy approaches to investigate the spatial and structural relationships between IGCs and chromatin. Our observations in HeLa cells demonstrate that IGCs establish physical connections with chromatin fibers. Furthermore, we show that the periphery of IGCs is enriched in decondensed chromatin domains and transcriptional sites. Quantitative analyses reveal that, upon α-amanitin treatment, the number of decondensed chromatin sites near IGCs is significantly reduced compared with untreated cells. In untreated conditions, a positive correlation emerges between IGC size and the abundance of adjacent decondensed chromatin regions. Based on these findings, we propose a model of IGC organization, considering their contacts with chromatin.</p>","PeriodicalId":13107,"journal":{"name":"Histochemistry and Cell Biology","volume":"164 1","pages":""},"PeriodicalIF":2.1,"publicationDate":"2026-03-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147485600","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Follicle-dependent differential localization of adipokines in the letrozole-induced hyperandrogenized mouse ovary.","authors":"Ayushmita Dutta, Guruswami Gurusubramanian, Vikas Kumar Roy","doi":"10.1007/s00418-026-02463-z","DOIUrl":"https://doi.org/10.1007/s00418-026-02463-z","url":null,"abstract":"<p><p>This study investigated whether ovarian adipokines exhibit uniform or stage-specific expression patterns across different follicular stages under hyperandrogenic conditions using a letrozole-induced polycystic ovary syndrome (PCOS) mouse model. Adult female mice received oral letrozole treatment for 21 days to induce hyperandrogenism, and ovarian tissues were analyzed by immunohistochemistry and western blot to examine the localization and expression of adiponectin (ADPN), adipoR1, adipoR2, leptin (Ob), leptin receptor (ObR), apelin (APLN), apelin receptor (APJ), chemerin, CMKLR1, and visfatin. Intense immunostaining for Ob, ObR, APJ, APLN, adipoR2, and visfatin was observed in primary, secondary, and Graafian follicles, whereas ADPN, adipoR1, and CMKLR1 showed reduced reactivity. In follicular cysts, adipoR2, APLN, APJ, and Ob were markedly upregulated compared with the corpus luteum of control ovaries, whereas ADPN, adipoR1, chemerin, CMKLR1, and ObR were downregulated. These findings indicate that hyperandrogenism disrupts adipokine signaling in a follicle-dependent manner, with differential expression patterns contributing to altered follicular maturation and cyst formation. The enhanced activation of adiponectin, apelin, and leptin signaling observed in cystic follicles may indicate disrupted adipokine-mediated regulation of ovarian physiology in letrozole-induced PCOS. Given the established roles of these adipokines in folliculogenesis and steroidogenesis, their dysregulation may contribute to follicular arrest and impaired ovarian function. These alterations are likely reflective responses to an altered endocrine and metabolic environment rather than direct causal mechanisms. Nonetheless, they may participate in the pathophysiological processes underlying cyst formation in PCOS.</p>","PeriodicalId":13107,"journal":{"name":"Histochemistry and Cell Biology","volume":"164 1","pages":""},"PeriodicalIF":2.1,"publicationDate":"2026-03-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147485675","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Vitamin D receptor suppresses pulmonary fibroblast activation by downregulating the TGF-β1/Smad signaling pathway.","authors":"Jialai Yang, Tangbing Xu, Rui Xu","doi":"10.1007/s00418-026-02462-0","DOIUrl":"10.1007/s00418-026-02462-0","url":null,"abstract":"<p><p>The vitamin D receptor (VDR) has been implicated in anti-inflammatory and antifibrotic effects, but its role in regulating TGF-β1/Smad signaling and fibroblast activation in pulmonary fibrosis remains unclear. This study investigates the regulatory effects of VDR on TGF-β1/Smad signaling and its impact on fibrogenic responses in lung fibroblasts. MRC-5 cells were treated with L-lactate sodium to generate a fibrotic model, and VDR and TGF-β1 expression were manipulated using plasmids and siRNA. Fibroblast activation, TGF-β1/Smad signaling, and ECM remodeling were assessed using qRT-PCR, western blot, and immunofluorescence, while cell proliferation, migration, invasion, oxidative stress, and inflammation were also evaluated. Lactate stimulation increased α-SMA and collagen I/III expression, confirming fibroblast activation. VDR overexpression reduced fibrotic markers, downregulated ECM-degrading enzymes (MMP2, MMP9), and upregulated TIMP-1, while inhibiting migration, invasion, and reducing ROS and inflammatory cytokines (IL-6, IL-1β). In contrast, VDR knockdown enhanced fibrotic marker expression and fibroblast activity. Phosphorylation of Smad2/3 decreased with VDR overexpression and increased with knockdown. TGF-β1 overexpression elevated fibrotic markers and Smad signaling, while TGF-β1 knockdown reduced these markers and alleviated the activated phenotype. Exogenous TGF-β1 treatment reversed the antifibrotic effects of VDR overexpression, linking VDR to TGF-β1/Smad signaling. VDR suppresses fibroblast activation and fibrotic responses in lung fibroblasts by downregulating the TGF-β1/Smad signaling pathway, highlighting its potential as a therapeutic target for pulmonary fibrosis.</p>","PeriodicalId":13107,"journal":{"name":"Histochemistry and Cell Biology","volume":"164 1","pages":""},"PeriodicalIF":2.1,"publicationDate":"2026-03-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147354865","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}